A central function of the human brain is to adapt to new situations based on past experience. Adaptation is reflected behaviorally by shorter reaction times to repeating or similar stimuli, and neurophysiologically by reduced neural activity in bulk-tissue measurements with fMRI or EEG. Several potential single-neuron mechanisms have been hypothesized to cause this reduction of activity at the macroscopic level. We here explore these mechanisms using an adaptation paradigm with visual stimuli bearing abstract semantic similarity. We recorded intracranial EEG (iEEG) simultaneously with spiking activity of single neurons in the medial temporal lobes of 25 neurosurgical patients. Recording from 4917 single neurons, we demonstrate that reduced event-related potentials in the macroscopic iEEG signal are associated with a sharpening of single-neuron tuning curves in the amygdala, but with an overall reduction of single-neuron activity in the hippocampus, entorhinal cortex, and parahippocampal cortex, consistent with fatiguing in these areas.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10148801PMC
http://dx.doi.org/10.1038/s41467-023-38190-5DOI Listing

Publication Analysis

Top Keywords

single-neuron mechanisms
8
single neurons
8
single-neuron
4
mechanisms neural
4
neural adaptation
4
adaptation human
4
human temporal
4
temporal lobe
4
lobe central
4
central function
4

Similar Publications

Flavor is the quintessential multisensory experience, combining gustatory, retronasal olfactory, and texture qualities to inform food perception and consumption behavior. However, the computations that govern multisensory integration of flavor components and their underlying neural mechanisms remain elusive. Here, we use rats as a model system to test the hypothesis that taste and smell components of flavor are integrated in a reliability-dependent manner to inform hedonic judgments and that this computation is performed by neurons in the primary taste cortex.

View Article and Find Full Text PDF

Intracranial electrical kilohertz stimulation has recently been shown to achieve similar therapeutic benefit as conventional frequencies around 140 Hz. However, it is unknown how kilohertz stimulation influences neural activity in the mammalian brain. Using cellular calcium imaging in awake mice, we demonstrate that intracranial stimulation at 1 kHz evokes robust responses in many individual neurons, comparable to those induced by conventional 40 and 140 Hz stimulation in both the hippocampus and sensorimotor cortex.

View Article and Find Full Text PDF

: The anterior cingulate cortex (ACC) is known for its involvement in various regulatory functions, including in the central control of feeding. Activation of local elements of the central glucose-monitoring (GM) neuronal network appears to be indispensable in these regulatory processes. Destruction of these type 2 glucose transporter protein (GLUT2)-equipped chemosensory cells results in multiple feeding-associated functional alterations.

View Article and Find Full Text PDF

Network hypersynchrony is emerging as an important system-level mechanism underlying seizures, as well as cognitive and behavioural impairments, in children with structural brain abnormalities. We investigated patterns of single neuron action potential behaviour in 206 neurons recorded from tubers, transmantle tails of tubers and normal looking cortex in 3 children with tuberous sclerosis. The patterns of neuronal firing on a neuron-by-neuron (autocorrelation) basis did not reveal any differences as a function of anatomy.

View Article and Find Full Text PDF

Mutant huntingtin protein decreases with CAG repeat expansion: implications for therapeutics and bioassays.

Brain Commun

November 2024

Department of Neurodegenerative Disease, Huntington's Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.

Huntington's disease is an inherited neurodegenerative disorder caused by a CAG repeat expansion that encodes a polyglutamine tract in the huntingtin (HTT) protein. The mutant CAG repeat is unstable and expands in specific brain cells and peripheral tissues throughout life. Genes involved in the DNA mismatch repair pathways, known to act on expansion, have been identified as genetic modifiers; therefore, it is the rate of somatic CAG repeat expansion that drives the age of onset and rate of disease progression.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!